Sepsis is a fetal immunological disorder and its complication worsens in the patients with hemodialysis which may increase the risk of death. In the present study, we aimed to investigate the effect of homeodomain-interacting protein kinase 3 (HIPK3) on inflammatory factors and oxidative stress markers in monocytes of rats with sepsis by regulating the c-Jun amino-terminal kinase (JNK)/c-Jun signaling pathway. A rat model of sepsis was initially established using cecal ligation and puncture (CLP) and was further identified by enlarged spleen tissues, inflammation, and oxidative stress. Monocytes were isolated from rats with CLP-induced sepsis. HIPK3 was observed to be downregulated while JUN was upregulated in monocytes from rats with CLP-induced sepsis. Furthermore, isolated monocytes were transduced with lentiviral vectors expressing HIPK3 or shRNA against HIPK3 to explore the effect of HIPK3 on viability and apoptosis of monocytes as well as inflammatory factors and oxidative stress markers. The obtained data exhibited that overexpression of HIPK3 or inhibition of the JNK signaling pathway enhanced proliferation, reduced apoptosis of monocytes, alleviated inflammation, and oxidative stress injury. Consistently, our results may provide evidence that HIPK3 could inhibit the JNK/c-Jun signaling pathway, thereby potentially retarding the progression of sepsis.

中文翻译：

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HIPK3通过JNK / c-Jun信号通路介导脓毒症大鼠模型中单核细胞的炎性细胞因子和氧化应激标志物。

脓毒症是一种胎儿免疫学疾病，血液透析患者的并发症会恶化，这可能会增加死亡风险。在本研究中，我们旨在通过调节c-Jun氨基末端激酶（JNK）/ c-来研究同源异域相互作用蛋白激酶3（HIPK3）对脓毒症大鼠单核细胞炎性因子和氧化应激标志物的影响Jun信号通路。最初使用盲肠结扎和穿刺（CLP）建立脓毒症的大鼠模型，并通过脾脏组织扩大，炎症和氧化应激进一步鉴定。从患有CLP诱导的败血症的大鼠中分离单核细胞。在患有CLP诱导的脓毒症的大鼠单核细胞中，观察到HIPK3被下调，而JUN被上调。此外，用表达针对HIPK3的HIPK3或shRNA的慢病毒载体转导分离的单核细胞，以研究HIPK3对单核细胞活力和凋亡以及炎性因子和氧化应激标志物的影响。获得的数据表明，HIPK3的过表达或JNK信号通路的抑制增强了增殖，减少了单核细胞的凋亡，减轻了炎症和氧化应激损伤。一致地，我们的结果可能提供证据，表明HIPK3可以抑制JNK / c-Jun信号通路，从而潜在地阻碍败血症的进程。获得的数据显示，HIPK3的过表达或JNK信号通路的抑制增强增殖，减少单核细胞的凋亡，减轻炎症和氧化应激损伤。一致地，我们的结果可能提供证据，表明HIPK3可以抑制JNK / c-Jun信号通路，从而潜在地阻碍败血症的进程。获得的数据表明，HIPK3的过表达或JNK信号通路的抑制增强了增殖，减少了单核细胞的凋亡，减轻了炎症和氧化应激损伤。一致地，我们的结果可能提供证据，表明HIPK3可以抑制JNK / c-Jun信号通路，从而潜在地阻碍败血症的进程。